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Jung, Kim, Min, Kang, Lee, Park, Kim, and Kwon: Acute-onset chronic inflammatory demyelinating polyneuropathy following hepatitis A virus infection
Case Report

Ann Clin Neurophysiol 2017;19(1):50-53.

Published online: 5 January 2017

DOI: https://doi.org/10.14253/acn.2017.19.1.50

Acute-onset chronic inflammatory demyelinating polyneuropathy following hepatitis A virus infection

Eui Sung Jung1, Ye Sel Kim2, Ju-Hong Min2, Kyusik Kang1, Jung Ju Lee1, Jong-Moo Park1, Byung-Kun Kim1, Ohyun Kwon1

1Department of Neurology, Nowon Eulji Medical Center, Eulji University School of Medicine, Seoul, Korea

2Department of Neurology, Samsung Medical center, School of Medicine, Sungkyunkwan University, Seoul, Korea

Correspondence to Ohyun Kwon Department of Neurology, Nowon Eulji Medical Center, Eulji University School of Medicine, 68 Hangeulbisuk-ro, Nowon-gu, Seoul 01830, Korea Tel: +82-2-970-8312 Fax: +82-2-974-7785 E-mail: koh1407@eulji.ac.kr

Received 25 March 201613 July 2016       Accepted 19 July 2016

Copyright © 2017 The Korean Society of Clinical Neurophysiology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

초록

An infection is less likely to elicit chronic inflammatory demyelinating polyneuropathy (CIDP) than Guillain-Barré syndrome. We here report a case of acute-onset CIDP following hepatitis A virus infection and briefly comment on the potential mechanisms regarding the induction and chronicity of autoimmunity after a viral infection.

Keywords: Polyradiculoneuropathy, Chronic inflammatory demyelinating, Guillain-Barre syndrome, Hepatitis A virus

REFERENCES

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Table 1.
Findings of nerve conduction studies (NCSs) at admission, hospital day 14, and hospital day 120
Nerve and stimulation site TL (ms) CMAP duration a (ms) CMAP amplitude (mV) NCV (m/s)
Motor NCSs        
Median (right)        
Wrist–APB 31.2/32.3/28.5 (≤ 3.6) 22.7/17.9/16.8 (≤ 6.6) 1.8/5.0/1.4 (≥ 5.0)  
Wrist–elbow   22.1/19.0/23.9 1.5/4.3/1.7 37/37/53 (≥ 50.0)
Ulnar (right)        
Wrist–ADM 11.7/11.9/9.9 (≤ 2.5) 13.3/14.4/12.7 (≤ 6.7) 1.6/3.3/7.8 (≥ 5.0)  
Wrist–elbow   11.4/13.6/15.1 1.5/3.1/1.7 28/28/60 (≥ 50.6)
Peroneal (right)        
Ankle–EDB 23.3/20.0/19.2 (≤ 4.8) 11.8/14.0/18.2 (≤ 7.6) 0.8/0.9/1.0 (≥ 4.0)  
Ankle–fibula   15.6/25.4/37.0 0.2/0.4/0.3 44/42/18 (≥ 41.7)
Tibial (right)        
Ankle 11.8/11.6/16.2 (≤ 5.1) 13.3/25.9/55.8 (≤ 8.8) 0.7/0.6/0.5 (≥ 5.0)  
Popliteal fossa   17.6/32.5/33 0.7/0.5/0.5 52/44/25 (≥ 40.6)
Nerve and stimulation site SNAP amplitude (μV) NCV (m/s)
Sensory NCSs        
Median (right), orthodromic method b        
Finger   NP/NP/NP (≥ 10)   -
Wrist   17.5/12.1/ND (≥ 10) 5 55/52/ND
Elbow   41.7/40.8/ND (≥ 10) 5 55/55/ND
Ulnar (right), orthodromic method b        
Finger   NP/NP/NP   -
Wrist   10.7/9.4/ND 55/5 6/ND (≥ 47.5)
Elbow   25.4/28.9/ND 55/5 4/ND (≥ 39.1)
Sural (right), antidromic method        
Lower leg   5.5/3.2/NP (≥ 6.0) 34/3 4/ND (≥ 34.7)
Dorsal sural (right), antidromic method        
Lower leg   NP/NP/NP (≥ 3.0)   -
Triplets indicate the values at admission/hospital day 14/hospital day 120. Numbers in parentheses are normal reference values. TL, terminal latency; CMAP, compound muscle action potential; NCV, nerve conduction velocity; APB, abductor pollicis brevis; ADM, abductor digiti min-imi; EDB, extensor digitorum brevis; SNAP, sensory nerve action potential; NP, no potential; ND, not done. a CMAP duration is defined as the interval between the onset of the first negative peak and the return to baseline after the last negative peak.
b The third sensory NCSs of the median and ulnar nerves were performed using the antidromic method.
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